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| August 15, 2004 - Urbanization, Migration and the Risk of Developing Schizophrenia: Part 1 |
In the classic research study by Faris and Dunham (1939), admission rates for schizophrenia in Chicago were demonstrated to be higher in inner city neighborhoods than towards the periphery of the city. The researchers suggested that the ‘etiologic’ factors may involve social isolation and social incohesion. Later researchers suggested that the higher rates could be attributed to ‘social’ or ‘downward drift.’ More recently, Lewis et al (1992) investigated geographic upbringing and incidence of schizophrenia using a cohort of over 49,000 male conscripts from the Swedish National Psychiatric Register. There was a significant linear trend of the diagnosis of schizophrenia to be more prevalent in those who had mostly lived in cities while they were growing up. However, this study was not able to discriminate between place of birth, place of upbringing and place of residence at the index period of psychosis.
Marcelis et al (1998), using the Dutch National Psychiatric Register and the Dutch Birth Register, demonstrated that urban birth was linearly associated with later psychosis. The strongest association was for narrowly defined schizophrenia and urban exposure. These investigators also found an interaction with gender in that the effect of urbanicity on all psychosis was greater in males than females.
In the largest study ever done, Mortensen et al (1999) investigated the effect of place and season of birth on risk of developing schizophrenia in a Danish cohort of 1.75 million. Again, there was a clear dose-response relationship between urbanicity and risk of admission for schizophrenia. Family history of schizophrenia did not explain or affect the results-the effect of urban birth was much larger than the effect of having a relative affected with schizophrenia. I believe such evidence is another significant challenge to the hegemony of biological reductionism, along with the findings of better outcomes in the developing countries than in the developed world and the large and significant overlap between the neurobiology of severe mental illness and profound and chronic fear/anxiety and stress, and it is incumbent upon those who espouse such restricted and narrow perspectives to make attempts to address these research findings and accord psychosocial factors with the weight such research has demonstrated they deserve. I realize reductionists can attribute the difference to such cellular processes as the risk of viral and bacterial exposure (particularly within the second trimester-see the research of Mednick et al) are greater during pregnancy in densely populated cities.
To make matters more complicated, theorists could attribute vulnerability to infection as arising from other factors such as preexisting CNS abnormalities, the immunological effects of exposure to prenatal stress, etc. Similarly, Susser et al (1996) demonstrated an association between malnutrition during pregnancy and later risk of schizophrenia, an area of study awaiting duplication. I would point to the other variables associated with poor diet, such as prenatal stress, lack of social support, educational deprivation, poverty, historical catastrophes, etc. For me the dialogue between more reductionistic theorists and theorists who do not marginalize significant psychosocial factors (eg, risk of infection in pregnant women may be significantly associated with poverty, social stress, etc) is what is crucial to the development of our field.
Research funding practices which consistently privilege such scientific research areas as psychopharmacology, neuroscience research which omits attention to known experiential and psychosocial variables which significantly impact on the neural areas of investigation (e.g., stress and ventriculomegaly) in favor of preexisting theoretical viewpoints (e.g., schizophrenia as a ‘brain disease’- as the term ‘chemical imbalance’-are empty signifiers knowing what we know about the CNS as being an open system) have no place in a ‘democracy’ of scientific inquiry (e.g., ISPS is a much needed antidote to the hegemony of reductionistic trends in research and treatment of severe mental illness). Just as geneticists studying schizophrenia have moved well beyond Mendelian single genes of strong effect to polygenic theories in which genes of small or moderate effect in interaction with key environmental events in a non-linear or dose-response relationship are suspected to play a role in the transmission of vulnerability (as opposed to inheritance of the ‘disorder’ itself) to the development of schizophrenia, reductionistic researchers need to understand that the human brain and neurogenetics are not closed systems, far from it, as such areas of research as neural plasticity, neuroimmunomodulation, molecular biological research on separation distress and attachment, and developmental psychobiology are demonstrating. Even with such a monogenic disorder as phenylketonuria (PKU), which is 100% genetic (eliminating all of the disease genes from the population would eradicate the illness), it could also be seen as 100% environmental since eliminating all phenylalanine from the diet would also eradicate the disease (this reminds me of Harvard social psychiatrist Leon Eisenberg’s point that the human brain is 100% biological and 100% social). As non-reductionists are quite aware, the division between genetic and environmental causation is not always clear (which reminds me of Robert Cancro’s quip that God did not create the universe according to university departmental lines).
In terms of distinguishing the effects of place of birth and place of upbringing, Astrup and Odegärd (1961) found a stronger effect for city upbringing. Pedersen and Mortensen (2001) demonstrated that schizophrenia risk increased with exposure and increasing degree of urbanization.
Researchers have proposed a host of possible ‘etiologic’ factors to account for these findings, including social class, obstetric complications, infectious disease, substance misuse, overcrowding, increased head injuries, noise levels, psychosocial stress, and social isolation. I find the latter two categories salient. Hare (1956) reported that social isolation, defined by the proportion of single households in a geographic area, is associated with increased rates of schizophrenia. Van Os et al (2000) observed in the Netherlands that single persons had a slightly higher risk of becoming psychotic if they lived in an area with fewer single persons than if they lived in an area with many other single persons. Jablensky et al (1997) demonstrated that marriage has a protective effect and that this was not simply a consequence of better-adapted males being able to marry. On a more personal clinical note, I have a person in my practice, one of many, whose positive psychotic symptoms increase significantly when he is alone and isolated. He was raised in a very emotionally sterile and deprived environment-should the psychotherapeutic or treatment situation duplicate this early environment his symptoms are significantly exacerbated (on an unconscious level, and now much more on a conscious level, he blames himself for the early emotional neglect and isolation he suffered through-he feels tremendous guilt for having had such a ‘destructive’ effect on his caregivers reflected in their withdrawal from him-the latter, in actuality, were immigrants to this country, trying to cope with racism and economic hardships-the issue of migration will be addressed in the second part of this multiple series on epidemiology and schizophrenia).
In summary, there is substantial evidence that urban birth/upbringing are associated with a higher risk of developing psychosis. The effect appears to be increasing and is stronger for narrowly defined schizophrenia and for males. Van Os et al (2001) ruled out the possibility that these are effects just associated with preexisting psychiatric vulnerabilities in a large Dutch study of the general population (N of 7,500).
Brian Koehler PhD
New York University
80 east 11th Street #339
New York NY 10003
212.533.5687
brian_koehler@psychoanalysis.net
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